Acute facial palsy (Bell’s palsy and important mimics)
Acute facial palsy is a common emergency presentation. Management in the ED focuses on rapid identification of life‑threatening causes (notably stroke), accurate bedside localisation (upper versus lower motor neurone pattern), prevention of corneal injury, and early disease‑modifying therapy when indicated.
Most isolated idiopathic peripheral facial palsies recover substantially, and uncomplicated adult Bell’s palsy does not usually need urgent specialist referral (NICE NG127). Use local stroke pathways when cortical signs are present (RCEM).
An approach
- Triage the patient and assess for life‑threatening features.
- Localise the lesion clinically (UMN vs LMN).
- Exclude stroke or other red flags.
- Protect the eye.
- Consider steroids and antivirals where appropriate.
- Arrange timely follow‑up and safety‑netting.
Anatomy and pathophysiological basis
- The facial (VII) motor nucleus in the pons receives bilateral cortical input to the upper face (frontalis) but predominantly contralateral input to the lower face. Therefore upper motor neuron (UMN; central) lesions classically spare forehead movement, while lower motor neuron (LMN; peripheral) lesions affect the entire ipsilateral hemiface including the forehead.
- The facial nerve traverses a narrow bony canal in the temporal bone; inflammatory swelling (for example viral neuritis in Bell’s palsy or zoster) can produce compressive neuropathy.
- Bell’s palsy is most likely due to reactivation of herpes simplex virus. Varicella‑zoster virus causes Ramsay Hunt syndrome (facial palsy with...